CCL4L1 is a CC chemokine that functions as a potent HIV-suppressive factor produced by CD8+ T cells 1. The protein binds to chemokine receptors CCR5, CCR1, and CCR2, exhibiting functional redundancy with its paralog CCL4, differing by only a single amino acid 2. Both proteins demonstrate comparable binding affinities and chemotactic properties, though CCL4L1 shows marginally greater HIV-1 inhibition in vitro 2. CCL4L1 blocks HIV entry through competitive binding to CCR5, downregulating receptor surface expression 1. The gene exists as variable copy number duplications on chromosome 17, ranging from 1-6 copies per diploid genome, yet copy number variation shows minimal impact on HIV susceptibility in adolescents 1. Clinically, CCL4L1 expression is dysregulated in systemic lupus erythematosus-associated renal disease, appearing downregulated in CD8+ T cells alongside aberrant cytotoxic signatures 3. During acute graft-versus-host disease, CCL4L1 expression in infiltrating donor CD8+ T cells contributes to a tissue invasion transcriptional signature enabling gastrointestinal tract occupancy 4. CCL4L1 is also implicated in gout pathogenesis as part of inflammatory response pathways 5. The gene's population genetics varies across ethnic groups and Native American populations 6.